ArticleJournal of virology2007
Relaxed repression of herpes simplex virus type 1 genomes in Murine trigeminal neurons.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- Genetic therapies for neurological diseases.Pharmacological reviews · 2026Review
- New model integrates innate responses, PML-NB formation, epigenetic control and reactivation from latency.EMBO reports · 2021Article
- Protocol Optimization for the Production of the Non-Cytotoxic JΔNI5 HSV Vector Deficient in Expression of Immediately Early Genes.Molecular therapy. Methods & clinical development · 2020Article
- Cellular Antisilencing Elements Support Transgene Expression from Herpes Simplex Virus Vectors in the Absence of Immediate Early Gene Expression.Journal of virology · 2018Article
- Herpes Simplex Virus Vectors for Gene Transfer to the Central Nervous System.Diseases (Basel, Switzerland) · 2018Review
- Engineered HSV vector achieves safe long-term transgene expression in the central nervous system.Scientific reports · 2017Article
- In vivo disruption of latent HSV by designer endonuclease therapy.JCI insight · 2016Article
- Latency Entry of Herpes Simplex Virus 1 Is Determined by the Interaction of Its Genome with the Nuclear Environment.PLoS pathogens · 2016Article
- Herpes simplex viral-vector design for efficient transduction of nonneuronal cells without cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Transcription of the herpes simplex virus 1 genome during productive and quiescent infection of neuronal and nonneuronal cells.Journal of virology · 2014Article
- In vitro Inactivation of Latent HSV by Targeted Mutagenesis Using an HSV-specific Homing Endonuclease.Molecular therapy. Nucleic acids · 2014Article
- Article
- Expression of herpes simplex virus 1 microRNAs in cell culture models of quiescent and latent infection.Journal of virology · 2014Article
- C-terminal trans-activation sub-region of VP16 is uniquely required for forskolin-induced herpes simplex virus type 1 reactivation from quiescently infected-PC12 cells but not for replication in neuronally differentiated-PC12 cells.Journal of neurovirology · 2013Article
- The molecular basis of herpes simplex virus latency.FEMS microbiology reviews · 2012Review
- A primary neuron culture system for the study of herpes simplex virus latency and reactivation.Journal of visualized experiments : JoVE · 2012Article
- Activities of ICP0 involved in the reversal of silencing of quiescent herpes simplex virus 1.Journal of virology · 2011Article
- Reversal of heterochromatic silencing of quiescent herpes simplex virus type 1 by ICP0.Journal of virology · 2011Article
- Viral genome silencing by neuronal sirtuin 1.Journal of neurovirology · 2011Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The expression of herpes simplex virus (HSV) genomes in the absence of viral regulatory proteins in sensory neurons is poorly understood. Previously, our group reported an HSV immediate early (IE) mutant (d109) unable to express any of the five IE genes and encoding a model human cytomegalovirus immediate early promoter-green fluorescent protein (GFP) transgene. In cultured cells, GFP expressed from this mutant was observed in only a subset of infected cells. The subset exhibited cell type dependence, as the fractions of GFP-expressing cells varied widely among the cell types examined. Herein, we characterize this mutant in murine embryonic trigeminal ganglion (TG) cultures. We found that d109 was nontoxic to neural cultures and persisted in the cultures throughout their life spans. Unlike with some of the cultured cell lines and strains, expression of the GFP transgene was observed in a surprisingly large subset of neurons. However, very few nonneuronal cells expressed GFP. The abilities of ICP0 and an inhibitor of histone deacetylase, trichostatin A (TSA), to activate GFP expression from nonexpressing cells were also compared. The provision of ICP0 by infection with d105 reactivated quiescent genomes in nearly every cell, whereas reactivation by TSA was much more limited and restricted to the previously nonexpressing neurons. Moreover, we found that d109, which does not express ICP0, consistently reactivated HSV type 1 (KOS) in latently infected adult TG cultures. These results suggest that the state of persisting HSV genomes in some TG neurons may be more dynamic and more easily activated than has been observed with nonneuronal cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.